Mechanistically, loss of ARID1A, along with PTEN deficiency, promotes prostate tumorigenesis through activation of NF-kB signaling, leading to CXCR2-mediated chemotaxis of MDSCs to shape the immunosuppressive TME, thus suggesting a potential therapeutic strategy of targeting ARID1A/NF-kB/CXCR2 axis in combination with ICB for advanced prostate cancer [77]. This evidence concerns the gene ARID1A and prostate carcinoma.